<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Txt>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE336nnn/GSE336205/suppl/GSE336205_genes_fpkm_expression.txt.gz</Txt><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE336nnn/GSE336205/</Other></files><type>primary</type></body><statusCodeValue>200</statusCodeValue><statusCode>OK</statusCode></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE336205</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>DUSP5 regulates ferroptosis in pancreatic cancer by down-regulating SCD1 expression via ERK1/2</name><description>This study aimed to explore the role and mechanism of DUSP5 in pancreatic ductal adenocarcinoma (PDAC). RNA sequencing was performed in DUSP5-overexpressing PANC-1 cells and control cells to identify differentially expressed genes. The results revealed that DUSP5 significantly downregulated stearoyl-CoA desaturase 1 (SCD1), a key enzyme involved in fatty acid metabolism and ferroptosis regulation. Our findings indicate that DUSP5 promotes ferroptosis and suppresses PDAC proliferation through the ERK1/2-SCD1 signaling pathway.</description><dates><publication>2026/06/28</publication></dates><accession>GSE336205</accession><cross_references><GSM>GSM9829997</GSM><GSM>GSM9829998</GSM><GSM>GSM9829995</GSM><GSM>GSM9829996</GSM><GSM>GSM9829993</GSM><GSM>GSM9829994</GSM><GPL>24676</GPL><GSE>336205</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>